Timeline to symptomatic Alzheimer's disease in people with Down syndrome as assessed by amyloid-PET and tau-PET: a longitudinal cohort study
Open accessAbstract
Background Adults with Down syndrome are at risk for Alzheimer's disease. Natural history cohort studies have characterised the progression of Alzheimer's disease biomarkers in people with Down syndrome, with a focus on amyloid β-PET and tau-PET. In this study, we aimed to leverage these well characterised imaging biomarkers in a large cohort of individuals with Down syndrome, to examine the timeline to symptomatic Alzheimer's disease based on estimated years since the detection on PET of amyloid β-positivity, referred to here as amyloid age, and in relation to tau burden as assessed by PET. Methods In this prospective, longitudinal, observational cohort study, data were collected at four university research sites in the UK and USA as part of the Alzheimer's Biomarker Consortium-Down Syndrome (ABC-DS) study. Eligible participants were aged 25 years or older with Down syndrome, had a mental age of at least 3 years (based on a standardised intelligence quotient test), and had trisomy 21 (full, mosaic, or translocation) confirmed through karyotyping. Participants were assessed twice between 2017 and 2022, with approximately 32 months between visits. Participants had amyloid-PET and tau-PET scans, and underwent cognitive assessment with the modified Cued Recall Test (mCRT) and the Down Syndrome Mental Status Examination (DSMSE) to assess cognitive functioning. Study partners completed the National Task Group-Early Detection Screen for Dementia (NTG-EDSD). Generalised linear models were used to assess the association between amyloid age (whereby 0 years equated to 18 centiloids) and mCRT, DSMSE, NTG-EDSD, and tau PET at baseline and the 32-month follow-up. Broken stick regression was used to identify the amyloid age that corresponded to decreases in cognitive performance and increases in tau PET after the onset of amyloid β positivity. Findings 167 adults with Down syndrome, of whom 92 had longitudinal data, were included in our analyses. Generalised linear regressions showed significant quadratic associations between amyloid age and cognitive performance and cubic associations between amyloid age and tau, both at baseline and at the 32-month follow-up. Using broken stick regression models, differences in mCRT total scores were detected beginning 2·7 years (95% credible interval [CrI] 0·2 to 5·4; equating to 29·8 centiloids) after the onset of amyloid β positivity in cross-sectional models. Based on cross-sectional data, increases in tau deposition started a mean of 2·7-6·1 years (equating to 29·8-47·9 centiloids) after the onset of amyloid β positivity. Mild cognitive impairment was observed at a mean amyloid age of 7·4 years (SD 6·6; equating to 56·8 centiloids) and dementia was observed at a mean amyloid age of 12·7 years (5·6; equating to 97·4 centiloids). Interpretation There is a short timeline to initial cognitive decline and dementia from onset of amyloid β positivity and tau deposition in people with Down syndrome. This newly established timeline based on amyloid age (or equivalent centiloid values) is important for clinical practice and informing the design of Alzheimer's disease clinical trials, and it avoids the limitations of timelines based on chronological age. Funding National Institute on Aging and the National Institute for Child Health and Human Development.
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Recent natural history studies have highlighted evidence of accelerated AD progression in people who have DSAD, including a more rapid development of tau spread as measured by positron emission tomography and plasma phospho-tau217, and enhanced rates of cortical thinning, after normalising for amyloid-β accumulation.
“Recent natural history studies comparing the development of AD in the general population and DSAD have highlighted evidence of accelerated AD progression in people who have DSAD. This includes a more rapid development of tau spread as measured by positron emission tomography and plasma phospho-tau217 [60, 68, 72], and enhanced rates of cortical thinning [37], after normalising for amyloid-β accum”
From Apolipoprotein E abundance is elevated in the brains of individuals with Down syndrome–Alzheimer’s disease (2025) · cites this paper as [60]
The Results report tau-PET increases at successive neurofibrillary-tangle stages after amyloid-β positivity in adults with Down syndrome. The paper does not establish that tau spreads faster than in the general population at comparable amyloid accumulation, and it does not report plasma phospho-tau217. Cortical thinning is cited separately in the citing sentence, so it is not attributed to this source. (LLM, conf=0.86)
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- Authors
- Schworer, E. K., Zammit, M. D., Wang, J., Handen, B. L., Betthauser, T., Laymon, C. M., Tudorascu, D. L., Cohen, A. D., Zaman, S. H., Ances, B. M., Mapstone, M., Head, E., Christian, B. T., Hartley, S. L., Aizenstein, H., Ances, B., Andrews, H., Bell, K., Birn, R., Brickman, A., Bulova, P., Cheema, A., Chen, K., Christian, B., Clare, I., Clark, L., Cohen, A., Constantino, J., Doran, E., Fagan, A., Feingold, E., Foroud, T., Handen, B., Harp, J., Hartley, S., Head, E., Henson, R., Hom, C., Honig, L., Ikonomovic, M., Johnson, S., Jordan, C., Kamboh, M. I., Keator, D., Klunk, W., Kofler, J., Kreisl, W., Krinsky-McHale, S., Lai, F., Lao, P., Laymon, C., Lee, J., Lott, I., Lupson, V., Mapstone, M., Mathis, C., Minhas, D., Nadkarni, N., O'Bryant, S., Parisi, M., Pang, D., Petersen, M., Price, J., Pulsifer, M., Rafii, M., Reiman, E., Rizvi, B., Rosas, D., Ryan, L., Schmitt, F., Schupf, N., Silverman, W., Tudorascu, D., Tumuluru, R., Tycko, B., Varadarajan, B., White, D., Yassa, M., Zaman, S., & Zhang, F.
- Affiliations
- University of Wisconsin–Madison (US)
- University of Pittsburgh (US)
- Washington University in St. Louis (US)
- Corresponding author
- Hartley, Sigan L
- ORCID
- Venue
- The Lancet Neurology
- Publisher
- Elsevier BV
- Published
- 2024-12
- Volume
- 23
- Issue
- 12
- Pages
- 1214-1224
- ISSN
- 1474-4422 (ISSN-L)
- PMC
- PMC12207984
- OpenAlex
- W4404555957
- Cited by
- 29
- References
- 32
- Citations by year
- 2026: 10 · 2025: 18 · 2024: 1
- FWCI
- 8.52
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
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- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (am, 170 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- The Lancet Neurology (acceptedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (P50 AG008702, U01 AG051406, K99AG084738)
- National Institute of Child Health and Human Development (U19 AG068054, U01 AG051412, P50 AG005681, P50 AG16537, P30 AG066519, P30 AG062715, P50 AG005133, P30 AG062421, T32 HD007489)
- University of Pittsburgh
- NIHR Cambridge Biomedical Research Centre
- National Institute for Health and Care Research
- National Institutes of Health
- National Center for Advancing Translational Sciences (UL1 TR001873, UL1 TR001414, UL1 TR001857, UL1 TR002373, UL1 TR002345)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- Down syndrome, Alzheimer's disease, amyloid PET, tau PET, amyloid-beta, tau burden, cognitive decline, dementia onset, Alzheimer's disease biomarkers, natural history (disease)
- MeSH terms
- Adult, Aged, Alzheimer Disease, Down Syndrome, Female, Humans, Longitudinal Studies, Male, Middle Aged, Prospective Studies, Cohort Studies, Amyloid beta-Peptides, tau Proteins, Disease Progression, Positron-Emission Tomography
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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